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Our work shows that the disease is rooted in a much broader network dysfunction
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The innate immune component of neuroinflammatory processes is primarily mediated by microglia, the resident macrophages of the CNS parenchyma, which release ROS, cytokines, and chemokines to attract peripheral immune cells or act as antigen-presenting cells
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Conversely, exogenous overexpression of GPX3 reduces kidney fibrosis and inhibits NADPH oxidase 2 and p38 mitogen-activated protein kinase activity [27]
